Impact of Helicobacter pylori- and Porphyromonas gingivalis-associated metabolic syndrome on local and systemic disorders.

: To the Editor, In their review, Straka et al. (2026) discussed the role of Helicobacter pylori infection (Hp-I) in gastric and oral pathologies and highlighted the benefits of Hp eradication at both gastric and oral sites when combined with concomitant periodontal therapy (Straka et al. 2026). In this context, it is worth further emphasizing the broader impact of Hp and Porphyromonas gingivalis (Pg) in metabolic syndrome (MetS) and in bacteria-driven local and systemic disorders. Hp-I remains highly prevalent worldwide, affecting more than 4.4 billion individuals (Kountouras 2025). As a Group I carcinogen, Hp plays a central role in gastric carcinogenesis through Correa's cascade, namely the progression from chronic gastritis to atrophy, intestinal metaplasia, dysplasia, and ultimately gastric cancer (Kountouras et al. 2008). In addition, Pg and its virulence factors, particularly gingipains, have also been implicated in this carcinogenic sequence (Salazar et al. 2013). Beyond its primary colonization of the gastric mucosa, Hp may also inhabit the oral cavity, including dental plaque, saliva, periodontal pockets, and especially dental pulp, thereby acting as an important extragastric reservoir (Momtaz et al. 2012). This oral-gastric axis may contribute to persistent infection, reinfection after eradication, and enhanced transmission (Momtaz et al. 2012). Likewise, the oral cavity is a major reservoir for Pg, which can disseminate systemically through the bloodstream and influence distant organs (Farrugia et al. 2021). Hp-I, together with alterations in the oral-gut microbiota, may disturb the microecological balance of this axis. Both Hp and Pg are strongly associated with oral diseases, particularly periodontitis, a dysbiosis-driven inflammatory disorder. Periodontitis itself has been linked to the initiation and progression of malignancies, especially oral cancers (Farhad et al. 2024). Although Hp and Pg colonize different anatomical niches, they appear to share important pathogenic mechanisms (Doulberis et al. 2021). A major determinant of Pg virulence is the gingipain family, a group of cysteine proteases involved in tissue destruction, immune evasion, and bacterial invasion. Emerging evidence also suggests that Hp may express functionally similar proteolytic enzymes, indicating overlapping or complementary pathogenic strategies (Doulberis et al. 2021). Notably, co-incubation of Hp and Pg has been reported to enhance Pg virulence, supporting a synergistic interaction that may aggravate both local and systemic disorders (Doulberis et al. 2021). These shared features underline the potential value of targeting both pathogens in antimicrobial strategies.